Location: Location not imported yet.Title: Deletion of the EP296R gene from the genome of highly virulent African swine fever virus Georgia 2010 does not affect virus replication or virulence in domestic pigs
|VUONO, ELIZABETH - University Of Wisconsin
|RAI, AYUSHI - Orise Fellow
|Spinard Iii, Edward
|VALLADARES, ALYSSA - Orise Fellow
Submitted to: Virus Research
Publication Type: Abstract Only
Publication Acceptance Date: 7/22/2022
Publication Date: 7/30/2022
Citation: Vuono, E., Ramirez Medina, E., Pruitt, S.E., Rai, A., Espinoza, N.N., Spinard Iii, E.J., Valladares, A., Velazquez Salinas, L., Gladue, D.P., Borca, M.V. 2022. Deletion of the EP296R gene from the genome of highly virulent African swine fever virus Georgia 2010 does not affect virus replication or virulence in domestic pigs. Virus Research. https://doi.org/10.3390/v14081682.
Interpretive Summary: African swine fever virus (ASFV) causes a devastating disease in swine, called African swine fever (ASF), that is currently spreading across Europe and Asia. There is no available vaccine for ASF, and currently only experimental live attenuated vaccines are derived from deletions of individual genes in the ASFV genome. In this study we were able to delete a a new protein and able to partially attenuate the virus.
Technical Abstract: African swine fever virus (ASFV) causes a lethal disease (ASF) in domestic pigs, African swine fever (ASF). ASF is currently producing a pandemic affecting pig production across Eurasia producing a shortage of food accessibility. ASFV is structurally com-plex, harboring a large genome encoding over 150 genes. A large proportion of those genes have not been studied, so their function largely relies on functional genomic predictions. One of them, EP296R, encodes for a predicted endonuclease, but has not been experimentally characterized. Here we report the development of a recombinant virus, ASFV-G-'EP296R, harboring the deletion of the EP296R gene from the genome of the highly virulent field isolate ASFV Georgia 2010 (ASFV-G). The recombinant ASFV-G-'EP296R replicates in primary swine macrophages with the same kinetics as the parental virus ASFV-G. Pigs experimentally infected by the intramuscular route with 102 HAD50 show a slightly protracted, although lethal, presentation of the disease when compared to that of animals inoculated with parental ASFV-G. Viremia titers in the ASFV-G-'EP296R infected animals closely followed the kinetics of presentation of clinical disease. Results presented here demonstrate that ASFV-G-'EP296R is not es-sential for the processes of ASFV replication in swine macrophages, nor is it radically involved in the process of disease production in domestic pigs.